These alcohol-induced changes in WAT with concurrent increases in liver fatty acid transport/binding proteins (cluster of differentiation 36 (CD36; Supplementary Fig. S3A) and adipose-specific FABP4 (Supplementary Fig. S3B)) facilitate increased uptake of adipose-derived circulating FFA, thereby contributing to the development of hepatic steatosis (Supplementary Figs. S3C & S3D). The gene discussed is CD36; the disease is Hepatic steatosis.